This invention relates generally to a device for stimulating cardiac tissue, and more particularly relates to an implantable cardiac rhythm management device capable of automatically detecting intrinsic and evoked response of a patient""s heart. The device of the present invention may operate in an automatic capture verification mode, wherein an accelerometer signal is utilized to identify heart sounds (S1 and S2) of the patient""s heart. The presence or absence of one or more of the heart sounds S1 and S2 in the accelerometer signal may indicate whether a stimulation pulse evokes a response by the patient""s heart. Further, the rhythm management device may automatically adjust the stimulation output in accordance with a step down stimulation protocol, wherein the presence of a predetermined heart sound indicates capture. Also, the device of the present invention may suspend the automatic capture verification mode if the patient""s physical activity level exceeds a predetermined threshold.
Cardiac rhythm management devices have enjoyed widespread use and popularity over the years as a means for supplanting some or all of an abnormal heart""s natural pacing functions. The various heart abnormalities remedied by these stimulation devices include total or partial heart block, arrhythmias, myocardial infarctions, congestive heart failure, congenital heart disorders, and various other rhythm disturbances within the heart. A cardiac rhythm management device generally includes a pulse generator that generates stimulation pulses to the heart. The pulse generator is electrically coupled to an electrode lead arrangement (unipolar or bipolar) positioned adjacent or within a pre-selected heart chamber for delivering stimulation pulses to the heart.
Regardless of the type of cardiac rhythm management device that is employed to restore the heart""s natural rhythm, all operate to stimulate excitable heart tissue cells adjacent to the electrode of the lead. Myocardial response to stimulation or xe2x80x9ccapturexe2x80x9d is a function of the positive and negative charges found in each myocardial cell within the heart. More specifically, the selective permeability of each myocardial cell works to retain potassium and exclude sodium such that, when the cell is at rest, the concentration of sodium ions outside of the cell membrane is significantly greater than the concentration of sodium ions inside the cell membrane, while the concentration of potassium ions outside the cell membrane is significantly less than the concentration of potassium ions inside the cell membrane.
The selective permeability of each myocardial cell also retains other negative particles within the cell membrane such that the inside of the cell membrane is negatively charged with respect to the outside when the cell is at rest. When a stimulus is applied to the cell membrane, the selective permeability of the cell membrane is disturbed and it can no longer block the inflow of sodium ions from outside the cell membrane. The inflow of sodium ions at the stimulation site causes the adjacent portions of the cell membrane to lose its selective permeability, thereby causing a chain reaction across the cell membrane until the cell interior is flooded with sodium ions. This process, referred to as depolarization, causes the myocardial cell to have a net positive charge due to the inflow of sodium ions. The electrical depolarization of the cell interior causes a mechanical contraction or shortening of the myofibril of the cell. The syncytial structure of the myocardium will cause the depolarization originating in any one cell to radiate through the entire mass of the heart muscle so that all cells are stimulated for effective pumping. Following heart contraction or systole, the selective permeability of the cell membrane returns and sodium is pumped out until the cell is re-polarized with a negative charge within the cell membrane. This causes the cell membrane to relax and return to the fully extended state, referred to as diastole.
In a normal heart, the sino-atrial (SA) node initiates the myocardial stimulation of the atrium. The SA node comprises a bundle of unique cells disposed within the roof of the right atrium. Each cell membrane of the SA node has a characteristic tendency to leak ions gradually over time such that the cell membrane periodically breaks down and allows an inflow of sodium ions, thereby causing the SA node cells to depolarize. The SA node cells are in communication with the surrounding atrial muscle cells such that the depolarization of the SA node cells causes the adjacent atrial muscle cells to depolarize. This results in atrial systole wherein the atria contract to empty blood into the ventricles.
The atrial depolarization from the SA node is detected by the atrioventricular (AV) node which, in turn, communicates the depolarization impulse into the ventricles via the Bundle of His and Purkinje fibers following a brief conduction delay. In this fashion, ventricular systole lags behind atrial systole such that the blood from the ventricles pumps through the body and lungs after being filled by the atria (the atrial and ventricular systole generally create the first heart sound S1). Atrial and ventricular diastole follow wherein the myocardium re-polarizes and the heart muscle relaxes in preparation for the next cardiac cycle (the atrial and ventricular diastole generally create the second heart sound S2). It is when this system fails or functions abnormally that a cardiac rhythm management device may be needed to deliver an electrical stimulation pulse for selectively depolarizing the myocardium of the heart so as to maintain proper heart rate and synchronization of the filling and contraction of the atrial and ventricular chambers of the heart.
The success of a stimulation pulse in depolarizing or xe2x80x9ccapturingxe2x80x9d the selected chamber of the heart hinges on whether the output of the stimulation pulse as delivered to the myocardium exceeds a threshold value. This threshold value, referred to as the capture threshold, is related to the electrical stimulation output required to alter the permeability of the myocardial cells to thereby initiate cell depolarization. If the local electrical field associated with the stimulation pulse does not exceed the capture threshold, then the permeability of the myocardial cells will not be altered enough and depolarization will not result. If, on the other hand, the local electrical field associated with the stimulation pulse exceeds the capture threshold, then the permeability of the myocardial cells will be altered sufficiently such that depolarization will result.
The ability of a rhythm management device to detect capture is desirable in that delivering stimulation pulses having energy far in excess of the patient""s capture threshold is wasteful of the rhythm management device""s limited power supply. In order to minimize current drain on the power supply, it is desirable to automatically adjust the device such that the amount of stimulation energy delivered to the myocardium is maintained at the lowest level that will reliably capture the heart. To accomplish this, a process known as capture verification must be performed wherein the rhythm management device monitors to determine whether an evoked depolarization occurs in the pre-selected heart chamber following the delivery of each stimulus pulse to the pre-selected chamber of the heart.
Changes in the capture threshold may be detected by monitoring the efficacy of stimulating pulses at a given energy level. If capture does not occur at a particular stimulation energy level which previously was adequate to effect capture, then it can be surmised that the capture threshold has increased and that the stimulation energy should be increased. On the other hand, if capture occurs consistently at a particular stimulation energy level over a relatively large number of successive stimulation cycles, then it is possible that the capture threshold has decreased such that the stimulation energy is being delivered at level higher than necessary to effect capture.
Past rhythm management devices have used electrode lead arrangements to sense an electrocardiogram signal from the patient""s heart and then utilize the sensed electrocardiogram signal during a capture verification mode, to determine if a stimulation pulse evokes a response by the heart. Fusion beats, artifacts, and/or noise may affect the electrocardiogram signal and may result in an erroneous conclusion concerning capture. As a result, the capture threshold may be identified at a lower amount than the actual threshold.
McClure et al. in U.S. Pat. No. 5,549,652 describes a system for automatic capture verification, wherein the system described by McClure et al. requires an implantable lead positioned within the heart and containing a cardiac wall motion sensor. In some instances it may desirable to replace the rhythm management device without replacing the implanted lead. Hence, unless the implanted lead contains a cardiac wall motion sensor, the system for autocapture verification described by McClure et al. is apparently ineffective as a replacement device, thereby limiting the versatility and applicability of the McClure et al. system. Thus, there is a need for a capture verification system that is unaffected by fusion beats, artifact and noise and which is not limited to a lead having specialized additional components. The present invention meets these and other needs that will become apparent from a review of the description of the present invention.
The present invention provides a cardiac rhythm management device capable of verifying that a stimulation output evokes a response in a selected region of the heart. The device of the present invention may function in a preset stimulation and/or autocapture mode, wherein a stimulation rate and timing interval of the device is preset. The rhythm management device generally includes a pulse generator, an accelerometer, and a controller. The pulse generator is electrically coupled to the controller and generates a stimulation pulse for delivery to at least one of an atrium and a ventricle of a heart. The accelerometer is also electrically coupled to the controller and transmits a signal to the controller, wherein the transmitted signal from the accelerometer is associated with accelerations of the heart and in particular is associated with fluid and myocardial accelerations of the heart. The controller includes means for identifying heart sounds or pulse pressure from the signal of the accelerometer over corresponding cardiac cycles and also includes means for determining whether the identified heart sound is associated with delivery of the stimulation pulse to the heart.
In the preferred embodiment, the accelerometer is electrically coupled to a band pass filter having a range of between 20-70 Hertz for filtering the""signal associated with fluid and myocardial accelerations of the heart. The controller may include a program or dedicated device of known suitable construction that defines a timing interval or window having a predefined duration, wherein the signal from the accelerometer is analyzed for the presence of increased pulse pressure or heart sounds during the timing interval or window. In an embodiment of the present invention, the controller determines a maximum output of the accelerometer signal relative to time during the window for at least one cardiac cycle. The midpoint or center of the timing interval or window is then set equal to the time at which the maximum output of the first cardiac cycle occurs.
The controller may utilize the signals from the accelerometer to determine whether capture occurs during a step down stimulation protocol. Various methods may be incorporated by the controller to identify heart sounds during the step down stimulation protocol. For example, during the timing interval or window the accelerometer signal may be rectified and low pass filtered and then compared for a substantial increase in amplitude. Likewise, the accelerometer signal may be signal processed to eliminate those portions of the signal associated with compressions, blood fluid motions and/or global cardiac wall accelerations and decelerations caused from cardiac activity along with motion artifacts and respiratory events. Alternatively, the signal energy may be analyzed or a cross correlation may be made between the signal output for known captured beats and the test stimulation beats.
In another embodiment of the invention, the controller determines a patient activity level and terminates the determination whether the identified heart sound is associated with delivery of the stimulation pulse to the heart when the patient activity level exceeds a predetermined amount. The controller determines from the accelerometer signal the patient activity level.
In use, the device determines whether a stimulation output is sufficient to evoke a response in a patient""s heart. An accelerometer is preferably positioned within the can or housing of the rhythm management device in order to obtain a globalized signal of the heart accelerations. Once a stimulation pulse is delivered having a predetermined output to a patient""s heart, the accelerometer signal is received and analyzed by the controller of the rhythm management device. The accelerometer signal includes variations in the signal associated with fluid and myocardial accelerations of the heart. The heart sounds S1 and/or S2 are identified for each cardiac cycle corresponding with the stimulation pulse. Once the accelerometer signal is analyzed, then the controller determines whether the identified heart sounds are associated with delivery of the stimulation pulse to the heart. In this manner capture of the heart may be verified. The advantages of the present invention will become readily apparent to those skilled in the art from a review of the following detailed description of the preferred embodiment especially when considered in conjunction with the claims and accompanying drawings in which like numerals in the several views refer to corresponding parts.